INVOLVEMENT OF IL-16 IN THE INDUCTION OF AIRWAY HYPERRESPONSIVENESS AND UP-REGULATION OF IGE IN A MURINE MODEL OF ALLERGIC-ASTHMA

Experiments were designed to investigate the role of IL-16 in a mouse model of allergic asthma, OVA-sensitized mice were repeatedly exposed to OVA or saline aerosols, Bronchoalveolar lavage fluid (BALF) was col lected after the last aerosol, and the presence of IL-16 was evaluated using a migration assay with human lymphocytes. Migration of lymphocy tes was significantly increased in the presence of cell-free BALF from OVA-challenged mice compared with BALF from saline-challenged control s, This response was significantly inhibited after addition of antibod ies to IL-16, demonstrating the presence of IL-16 in BALF of OVA-chall enged animals, Immunohistochemistry was performed and revealed IL-16 i mmunoreactivity particularly in airway epithelial cells but also in ce llular infiltrates in OVA-challenged mice. IL-16 immunoreactivity was absent in nonsensitized animals; however, some reactivity was detected in epithelial cells of sensitized but saline-challenged mice, suggest ing that sensitization induced IL-16 expression in airway epithelium. Treatment of mice with antibodies to IL-16 during the challenge period significantly suppressed up-regulation of OVA-specific IgE in OVA-cha llenged animals, Furthermore, antibodies to IL-16 significantly inhibi ted the development of airway hyper-responsiveness after repeated OVA inhalations, whereas the number of eosinophils in bronchoalveolar lava ge or airway tissue was not affected, In conclusion, IL-16 immunoreact ivity is present in the airways after sensitization, After repeated OV A inhalation, IL-16 immunoreactivity is markedly increased and IL-16 i s detectable in BALF, Furthermore, IL-16 plays an important role in ai rway hyper-responsiveness and up-regulation of IgE but is not importan t for eosinophil accumulation in a mouse model of allergic asthma.